thyroid Flashcards
associated with hyper metabolic and hyperadrenergic symptoms (tachycardia, palpitations, insomnia, anxiety, tremor, heat intolerance, weight loss)
hyperthyroidism
treats hyperthyroidism by inhibiting thyroid peroxidase and 5’ deiodinase - decreasing conversion of T4 into T3
propylthiouracil (PTU)
actions of thyroxine
growth: bone in children, brain in fetal life and 1st year of postnatal life (lack thyroid hormone in fetal life cretinism)
ADR: severe hepatotoxicity, maculopapular rash, drug induced lupus, agranulocytosis
propylthiouracil
can be used in 1st tri
ADR: drug induced lupus, 1st trimester teratogen (b/c of extensive protein binding), cholestatic dysfunction
methimazole
used in 2nd and 3rd trimester of pregnancy tp avoid PTU liver toxicity in later trimesters
methimazole
uses for PTU and methimazole
1) graves
2) radioactive iodine conjunction
3) preoperative preparation of thyroid gland
4) thyrotoxic crisis
associated with dry brittle hair, lethargy, fatigue, weakness, decreased BMR, cold intolerance, myxedema, lack appetite, weight gain
Hypothyroidism
untreated hypothyroidism can lead to
myxedema coma
treats hypothyroidism and hashimotos
levothyroxine (synthetic T4)
ADR: hyperthyroidism, tachycardia, heat intolerance, tremors
levothyroxine
used to tx myxedema coma (emergency)
ADR: avoid in heart dz
liothyronine sodium
thyroid hormone biologically available in tissue
T3
growth: bones in children, brain in fetal life and 1st few years postnatal life (lack of thyroid hormone in fetal life - cretinism) and effects on cardio (increase HR, BF, CO, contraction))
actions of thyroxine
thyroid hormone synthesis
1) uptake of iodide (trapping)
2) iodide organification : oxidation and iodination
3) coupling of MIT and DIT
4) secretion of thyroid hormones
5) conversion of T4 to T3 (peripheral conversion)
combo of two DIT less potent 75% protein bound .04% exists in free form converted to T3 in the peripheral tissues, liver, and kidneys
T4
combo of one MIT and one DIT 4 times more potent 25% bound .4% exists in free form binds actively to nuclear receptor (active form)
T3
protrusion of the eyeball
ulceration of cornea
stretches the optic nerve to damage vision
exophthalmos
TSH decrease
Free T3 increase
Free T4 increase
RAI increase
Graves dz
TSH decrease
Free T3 increase
Free T4 increase
RAI decrease
sub acute thyroiditis
TSH decrease
Free T3 increase
Free T4 increase
RAI decrease/normal
exogenous T3 or T4
TSH increase
Free T3 decrease
Free T4 decrease
primary hypothyroidism
TSH normal
Free T3 normal
Free T4 normal
RAI normal
total T4 increase
pregnancy TBG increase
trapped by thyroid gland
radiation destruction of thyroid parenchyma
MOA of RAI
Uses: graves dz: px with heart dz (after making them euthyroid) and toxic nodular goiter
RAI
antithyroid drugs should be discontinued 1 week before and resumed 3 days after 131I therapy (decrease efficacy)
iodides should be avoided to prevent competition in uptake
Admin of RAI
avoid in pregnancy and lactating mothers
can cause hypothyroidism
RAI
increase delayed hypothyroidism
increase stomach, kidney, breast cancer
increase radiation
disadvantages of RAI
no risk of surgery
decrease cost
advantages of RAI
competitively inhibiting the NIS (inhibit uptake of iodine)
large doses can overcome competitive inhibition
ionic inhibitors
ionic inhibitors
thiocyanate
perchlorate
fluoroborate = perchlorate
used to tx iodide induced hyperthyroidism like amiodarone induced thyrotoxicosis
perchlorate
10 times x thiocyanate
aplastic anemia
perchlorate
inhibits the organification of iodine
thiocyanate
iodides
lugols solution
saturated solution of K iodide (KISS)
K iodide
MOA
1) imitation its own transport
2) inhibition of synthesis of iodotyrosine and iodothyronines
3) inhibition of the release of thyroid hormone
4) reduces vascularity and size
iodides
uses
1) preoperative preparation of thyroid gland
2) thyrotoxic crisi - hyper metabolic state
3) radioactive iodine fallout
iodides
competes with RAI
not used long term due to escape
vascularity is reduced
gland becomes firmer
iodides
ADR: marked sensitivity to iodide (allergy), IODISM: chronic intoxication with iodide (brassy taste in mouth), pulmonary edema, in pregnancy: iodide cross placenta and cause fetal goiter
iodides
adjunct therapy
1) beta blockers without ISA - propanolol - use to control hyperthyroidism
2) dexamethasone
3) iopanic acid and sodium ipodate
4) cholestyramine
5) rituximab
beta blockers with ISA CI in hyperthyroidism
carteolol labetalol penbutolol pindolol acebutolol
thyrotoxicosis but exaggerated hyperthyroidism
thyroid storm
tx for thyroid storm
1) antithyroid - propylthiouracil
2) B adrenergic blockers - tx HTN and increase HR
3) hydrocortisone - prevnts shock, inhibits peripheral conversion T4 -T3
4) oral iodides - iopanic acid and sodium update
5) tx underlying precipitating illness
